期刊
PLANT CELL
卷 22, 期 4, 页码 1313-1332出版社
OXFORD UNIV PRESS INC
DOI: 10.1105/tpc.109.069609
关键词
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资金
- National Basic Research Program of China [2006CB100100]
- National High Technology Research and Development Program of China 863 [2008AA022304]
- U.S. Department of Energy/Energy Biosciences [DE-FG02-04ER15616]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM047850] Funding Source: NIH RePORTER
The plasma membrane H+-ATPase (PM H+-ATPase) plays an important role in the regulation of ion and metabolite transport and is involved in physiological processes that include cell growth, intracellular pH, and stomatal regulation. PM H+-ATPase activity is controlled by many factors, including hormones, calcium, light, and environmental stresses like increased soil salinity. We have previously shown that the Arabidopsis thaliana Salt Overly Sensitive2-Like Protein Kinase5 (PKS5) negatively regulates the PM H+-ATPase. Here, we report that a chaperone, J3 (DnaJ homolog 3; heat shock protein 40-like), activates PM H+-ATPase activity by physically interacting with and repressing PKS5 kinase activity. Plants lacking J3 are hypersensitive to salt at high external pH and exhibit decreased PM H+-ATPase activity. J3 functions upstream of PKS5 as double mutants generated using j3-1 and several pks5 mutant alleles with altered kinase activity have levels of PM H+-ATPase activity and responses to salt at alkaline pH similar to their corresponding pks5 mutant. Taken together, our results demonstrate that regulation of PM H+-ATPase activity by J3 takes place via inactivation of the PKS5 kinase.
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